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. 2019 Sep 3;10:3967. doi: 10.1038/s41467-019-11951-x

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© The Author(s) 2019

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 2 — Kidney pathology analysis and neuroimaging. Light and transmission electron microscopy (TEM) of kidney sections of patients with GON7 (a, b) or YRDC mutations (c, d). a Individual A.II-3 displays a retracted glomerulus with a focal segmental glomerulosclerosis lesion at the vascular pole (black arrow) and tubular dilations (black star) (PAS; ×200 magnification). b Individual B.II-4 displays diffuse mesangial sclerosis with tiny, retracted and sclerosed glomeruli (black arrow) with dilated tubes surrounded by flat epithelial cells (black star) and interstitial fibrosis (H&E; ×400 magnification). c Individual F.II-1 displays a marked glomerular tuft collapsing (arrowhead) surrounded by a layer of enlarged and vacuolized podocytes (black arrows) (PAS stain; ×400 magnification, scale bar, 10 µm). d TEM of individual G.II-1 shows diffuse foot process effacement (FPE; black arrow), a classical hallmark of nephrotic syndrome, along a glomerular basement membrane (GBM) with abnormal folded and laminated segments (yellow stars), alternating with others with normal appearance. P podocyte, RBC red blood cell. Scale bar, 2 µm. Brain MRI of patients with GON7 (e, f) and YRDC mutations (i–n). e, f Brain MRI abnormalities in individual B.II-4 at 5 years. Sagittal T1-weighted image (e) shows important cortical subtentorial atrophy as well as corpus callosal (arrow) and cerebellar atrophy (arrowhead). The axial T2-weighted image (f) shows abnormal myelination and ventricular dilatation (red arrow). g, h Brain MRI of a 5-year old control showing sagittal T1 (g) and axial T2 (h) weighted images. i–l Brain MRI abnormalities in individual F.II-1 at 5 months (i, j) and 11 months (k, l). Sagittal T2-weighted image shows normal pattern at 5 months (i) evolving to a progressive major cerebellar (arrowhead) and cortical atrophy with a very thin corpus callosum (arrow) at 11 months (k). The axial T2-weighted image is normal at 5 months (j) but shows a very marked abnormality of myelination and cortical atrophy (red arrow) at 11 months (l). m, n Brain MRI abnormalities in individual G.II-2 at 1 month. Sagittal T2 (m) and axial T2 (n) weighted images show gyral anomalies with marked frontal gyral simplification (red arrow) and myelination delay